Use of pentagastrin to inhibit gastric acid secretion or as a diuretic
a technology of pentagastrin and gastric acid, which is applied in the field of physiological disorders, can solve problems such as ulceration and inflammation of the gastrointestinal tract, and achieve the effects of prolonging the effect, increasing the acid secretion, and increasing the efficacy
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example 1
Inhibition of Pentagastrin-Induced Gastric Acid Secretion by Intravenous Pantoprazole: A Dose-Response Study
[0070] The purpose of this study was to compare the gastric acid inhibitory ability of increasing doses of intravenous (i.v.) pantoprazole with that of i.v. famotidine and placebo. Pentagastrin was infused continuously in healthy subjects as a model for patients with Zollinger-Ellison syndrome.
[0071] In brief, pentagastrin (1 μg / kg / h) was infused to stimulate maximum acid output in 39 subjects over a 25-h period. After 60 min of pentagastrin infusion, subjects received a single dose of i.v. pantoprazole (20, 40, 80, or 120 mg), i.v. famotidine (20 mg), or saline placebo. The variables measured were onset of response (time until acid output fell to <10 mEq / h), duration of response (time acid output remained <10 mEq / h), and cumulative acid output over 24 h.
[0072] All doses of i.v. pantoprazole produced a dose-dependent suppression of acid output to 90% in all subjects for <21...
example 2
Discovery of Gastrin Receptors in the Kidney Reveals Hormonal Coupling of Digestion and Excretion
[0102] Ingestion of a meal results in acute changes in renal function necessary to handle absorbed nutrients (Pullman (1954) J. Lab. Clin. Med. 44: 320-332; Jolliffe and Smith (1931) Am. J. Physiol. 99: 101-107; Schoolwerth et al. (1975) Kidney Int. 7: 397-404). However, the mechanism for communication between the digestive and renal systems has never been established. In this example, we report that receptors for gastrin, cholecystokinin type B / gastrin receptors (CCKB / gastrin), are expressed at high levels in the kidney and that gastrin, elevated by either a meal or direct renal infusion, stimulates an increase in urinary Na+ excretion and urine volume that is inhibited by the CCKB / gastrin receptor-specific antagonist, L-365,260 (Lotti and Chang (1989) Eur. J. Pharmacol. 163: 273-279). Gastrin stimulated excretion of sodium and water and its reversal by L-365,260 are paralleled by CCKB...
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